Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to test if a benzodiazepine would enhance or hinder the therapeutic effects of exposure, immediate and delayed effects of alprazolam on flight phobics were assessed by questionnaires and ambulatory physiological recording. Physiological measures included heart rate, skin conductance level and fluctuations, finger temperature, respiratory sinus arrhythmia, and various respiratory measures derived from two bands calibrated for each subject. Twenty-eight women with flying phobia flew twice at a 1-week interval. One and a half hours before flight 1, 14 randomly assigned phobics received double-blind 1 mg of alprazolam and 14 received placebo. On flight 1, alprazolam reduced self-reported anxiety (5.0 vs 7.4) and symptoms (5.3 vs 3.6) more than placebo, but induced an increase in heart rate (114 vs 105 bpm) and respiratory rate (22.7 vs 18.3 breaths/min). Before flight 2, the alprazolam group did not expect to be more anxious than the placebo group (6.7 vs 6.5), but in fact indicated more anxiety during flight (8.5 vs 5.6), and a substantial increase in panic attacks from flight 1 to flight 2 (7% vs 71%). Heart rates in the alprazolam group increased further (123 bpm). Results indicate that alprazolam increases physiological activation under acute stress conditions and hinders therapeutic effects of exposure in flying phobia.
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PMID:Acute and delayed effects of alprazolam on flight phobics during exposure. 929 3

Thought Field Therapy (TFT) is a self-administered treatment developed by psychologist Roger Callahan. TFT uses energy meridian treatment points and bilateral optical-cortical stimulation while focusing on the targeted symptoms or problem being addressed. The clinical applications of TFT summarized included anxiety, adjustment disorder with anxiety and depression, anxiety due to medical condition, anger, acute stress, bereavement, chronic pain, cravings, depression, fatigue, nausea, neurodermatitis, obsessive traits, panic disorder without agoraphobia, parent-child stress, phobia, posttraumatic stress disorder, relationship stress, trichotillomania, tremor, and work stress. This uncontrolled study reports on changes in self-reported Subjective Units of Distress (SUD; Wolpe, 1969) in 1,594 applications of TFT, treating 714 patients. Paired t-tests of pre- and posttreatment SUD were statistically significant in 31 categories reviewed. These within-session decreases of SUD are preliminary data that call for controlled studies to examine validity, reliability, and maintenance of effects over time. Illustrative case and heart rate variability data are presented.
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PMID:Thought Field Therapy clinical applications: utilization in an HMO in behavioral medicine and behavioral health services. 1152 9

The literature to date that examines the biology of the acute stress reactions suggests that relatively lower baseline cortisol is associated with the development of PTSD. This is particularly informative because of the ongoing controversy surrounding baseline cortisol in PTSD. Studies have found low baseline cortisol, normal range, and elevated baseline cortisol in chronic PTSD, and it has been unclear whether this reflects methodologic differences across studies or true heterogeneity within the disorder. Thus, the few studies to date support the finding of low-normal baseline cortisol in chronic PTSD and suggest that it is a pre-existing functional trait. Whether it plays an etiologic role or is an epiphenomenon of some other process is unclear. What does seem clear, however, is that this characteristic is relatively nonspecific to PTSD, given the fact that low cortisol has been observed in multiple subject populations, including normal individuals under chronic stress as well as chronic medical conditions (for review see [23]). For example, it is possible that reduced baseline cortisol reflects the net result of input to the hypothalamus from cortical and subcortical regions of the brain linked to increased vigilance, sensitization to trauma because of prior traumatic experiences, or genetic factors. For example, primate studies have demonstrated persistent alterations in HPA axis functioning in animals reared by mothers living in moderately stressful conditions [24]. The development of PTSD is associated with sensitization of the startle response. Because the neurobiology of startle is well characterized, this finding implicates a role for specific neurocircuitry in PTSD [25]. Non-habituation of the startle response in PTSD appears related to sensitization specifically to contextual cues (i.e., the environment) that signal the presence of potential threat of danger-related fears [26]. This may be the neurobiological correlate to the over-generalization seen in PTSD that distinguishes the disorder from a simple trauma-induced phobia. The bed nucleus of the stria terminalis (BNST) is specifically implicated from preclinical research in the mediation of context-dependent cues [1]. Treatments that result in down-regulation of the BNST are therefore of particular interest in therapeutic models of prevention after trauma. The fact that a number of vulnerability factors associated with increased risk for developing PTSD are also likely to be biologically based (e.g., a genetic component, prior psychiatric history, prior family of history of psychiatric disorder), provides further evidence in support of a role for psychobiological factors in producing PTSD. Nevertheless, the considerable overlap on these measures between those who will develop PTSD, and those who eventually recover spontaneously, belies any attempt to identify any single or pathognomonic biological marker for risk. For now, the standard of care in predicting level of symptomatology and prognosis in the acute setting continues to be based on careful, informed, serial assessments of symptoms and functioning. Because the capacity to learn from and adapt to adverse conditions are essential to the survival of any species, understanding the neurobiological pathways that mediate learning from traumatic experiences in an adaptive way is as important as understanding the etiology of PTSD and other trauma-related maladaptive consequences. Biological models that trace the causal cascade of post-traumatic events in the brain and neuroendocrine systems may offer a multiplicity of possibilities for intervention. It is well established that conditioned responses are robust and persistent. Moreover, the primary mechanism of habituation is overlearning rather than extinction. Interventions that promote overlearning may therefore prove to be the most powerful and efficient preventative treatments. The therapeutics literature supports this hypothesis, in that brief psychosocial interventions based on sophisticated cognitive-behavioral models have proven effective in reducing suffering, symptom severity, and chronicity in individuals presenting with acute PTSD symptoms [27-29]. No acutely administered pharmacologic treatment to date has been shown effective in accelerating the process of recovery or in preventing the development of chronic PTSD. However, pharmacologic interventions that would prevent sensitization of circuits related to context-dependent threat perception, dysregulation of affect, and/or dysregulation of normal circadian rhythms are of theoretical interest and deserve further study.
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PMID:Psychobiology of the acute stress response and its relationship to the psychobiology of post-traumatic stress disorder. 1213 6

This article reviews the existing evolutionary perspectives on the acute stress response habitual faintness and blood-injection-injury type-specific phobia (BIITS phobia). In this article, an alternative evolutionary perspective, based on recent advances in evolutionary psychology, is proposed. Specifically, that fear-induced faintness (eg, fainting following the sight of a syringe, blood, or following a trivial skin injury) is a distinct Homo sapiens-specific extreme-stress survival response to an inescapable threat. The article suggests that faintness evolved in response to middle paleolithic intra-group and inter-group violence (of con-specifics) rather than as a pan-mammalian defense response, as is presently assumed. Based on recent literature, freeze, flight, fight, fright, faint provides a more complete description of the human acute stress response sequence than current descriptions. Faintness, one of three primary physiological reactions involved in BIITS phobia, is extremely rare in other phobias. Since heritability estimates are higher for faintness than for fears or phobias, the author suggests that trait-faintness may be a useful complement to trait-anxiety as an endophenotype in research on the human fear circuitry. Some implications for the forthcoming Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition as well as for clinical, health services, and transcriptomic research are briefly discussed.
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PMID:Freeze, flight, fight, fright, faint: adaptationist perspectives on the acute stress response spectrum. 1533 64

In this prospective longitudinal study, the authors examined the relationship between reduced specificity in autobiographical memory retrieval and the development of depression, posttraumatic stress disorder (PTSD), and specific phobia after injury in an assault. Assault survivors (N = 203) completed the Autobiographical Memory Test (J. M. G. Williams & K. Broadbent, 1986) at 2 weeks after the trauma as well as structured clinical interviews at 2 weeks and 6 months. Participants with acute stress disorder or major depression at 2 weeks, but not those with phobia, retrieved fewer specific autobiographical memories than those without the respective disorder. Reduced memory specificity at 2 weeks also predicted subsequent PTSD and major depression at 6 months over and above what could be predicted from initial diagnoses and symptom severity. Moderator analyses showed that low memory specificity predicted later depression in participants with prior episodes of major depression but not in those without prior depression. Mediation analyses suggested that rumination partly mediated and perceived permanent change fully mediated the effects of low memory specificity on posttrauma psychopathology at follow-up.
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PMID:Reduced autobiographical memory specificity predicts depression and posttraumatic stress disorder after recent trauma. 1837 20

There is a rapidly accumulating body of evidence regarding the influential role of early life stress (ELS) upon medical and psychiatric conditions. While self-report instruments, with their intrinsic limitations of recall, remain the primary means of detecting ELS in humans, biological measures are generally limited to a single biological system. This paper describes the design, rationale and feasibility of a study to simultaneously measure neuroendocrine, immune and autonomic nervous system (ANS) responses to psychological and physiological stressors in relation to ELS. Five healthy university students were recruited by advertisement. Exclusion criteria included chronic medical conditions, psychotic disorders, needle phobia, inability to tolerate pain, and those using anti-inflammatory medications. They were clinically interviewed and physiological recordings made over a two-hour period pre, during and post two acute stressors: the cold pressor test and recalling a distressing memory. The Childhood Trauma Questionnaire and the Parental Bonding Index were utilised to measure ELS. Other psychological measures of mood and personality were also administered. Measurements of heart rate, blood pressure, respiratory rate, skin conductance, skin blood flow and temporal plasma samples were successfully obtained before, during and after acute stress. Participants reported the extensive psychological and multisystem physiological data collection and stress provocations were tolerable. Most (4/5) participants indicated a willingness to return to repeat the protocol, indicating acceptability. Our protocol is viable and safe in young physically healthy adults and allows us to assess simultaneously neuroendocrine, immune and autonomic nervous system responses to stressors in persons assessed for ELS.
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PMID:Design, rationale and feasibility of a multidimensional experimental protocol to study early life stress. 2969 66